BBB Seminar: Sandra Kleinau

Sandra Kleinau
Department of Cell and Molecular Biology, Biomedical Center, Uppsala University, Sweden

Knowledge on how self-reactive B lymphocytes are regulated in the periphery is limited. In the context of innate immune signaling it has become increasingly clear that various signals from the complement system play important roles in B cell immune responses and tolerance. The effect of complement on B cells is mediated predominantly by two distinct complement receptors, type 1 (CR1) and type 2 (CR2), which, when occupied with complement fragments opsonized to antigen, can induce inhibitory signals. Another inhibitory receptor expressed on B cells is Fc gamma receptor IIb (FcgRIIb), which upon ligation with IgG immune complexes negatively regulates activating signals transduced by the B cell receptor. Lack of signals from CR1, CR2 or FcgRIIb can result in alterations in B cell responses and in self-tolerance, allowing survival and activation of self-reactive B cells leading to autoimmunity. Rheumatoid arthritis (RA) is an autoimmune disease where self-reactive B cells have a central role in the disease pathogenesis, as they are a critical link to the autoantibody production observed. However, the B cells may also contribute to the autoimmune reaction by secretion of immune modulating cytokines and presentation of antigen. In this presentation I will discuss how B cell inhibitory receptors influence collagen-induced arthritis in mice and B cells in RA patients. The understanding of negatively regulatory proteins and their control of self-reactive B cells will help to identify mechanisms involved in the pathophysiology of antibody-mediated autoimmune disorders such as RA.

Chair: Anne Isine Bolstad, Department of Clinical Dentistry

Arranged in cooperation with the research group Oral infections and inflammations at the Department of Clinical Dentistry and the Bergen Research School in Inflammation (BRSI)